1. A variant of DC-SIGN gene promoter associated with resistance to HIV-1 in serodiscordant couples in Burkina Faso
Thérèse Samdapawindé KAGONÉ ; Cyrille BISSEYE ; Albert Théophane YONLI ; Tegwindé Rebeca COMPAORÉ ; Jean Baptiste NIKIÉMA ; Jacques SIMPORE ; Thérèse Samdapawindé KAGONÉ ; Nicolas MÉDA ; Jean TESTA ; Dramane KANIA ; Cyrille BISSEYE ; Virginio PIETRA ; Comlan DE SOUZA
Asian Pacific Journal of Tropical Medicine 2014;7(S1):S93-S96
Objective: To study the involvement of variations in 4 genes associated with susceptibility and/or protection against HIV-1 in serodiscordant couples in Burkina Faso, namely, genes encoding HLA-B57, interferon regulatory factor 1 (IRF1), dendritic cell-specific ICAM3-grabbing nonintegrin (DC-SIGN) and CCR5 delta 32 (CCR5δ32). Methods: Two DC-SIGN and two IRF1 single nucleotide polymorphisms (SNPs) as well as HLA-B57*01 and CCR5δ 32 alleles were genotyped in 51 serodiscordant couples in Burkina Faso. DC-SIGN, IRF1 and HLA-B57*01 genotyping was carried out by real time PCR using TaqMan assays (Applied Biosystems, USA and Sacace Biotechnologies, Italy). CCR5δ 32 deletion was investigated by PCR. Results: The two SNPs of DC-SIGN promoter showed a significant genotypic difference in serodiscordant couples. After multivariate analysis, only the association between DC-SIGN rs2287886 and HIV-1 remained significant (P<0.01). No association was found between IRF1 SNPs and HIV-1 infection. CCR5δ 32 wild type allele was found in 100% of serodiscordant couples. A high frequency of HLA-B57*01 allele was found in the HIV-positive (78%) compared with HIV-negative group (51%), however this difference was no longer significant after the correction of the sex confounding effect in the logistic regression model. Conclusions: Our study suggests a protective role of a variation of DC-SIGN promoter and genetic resistance to HIV-1 in serodiscordant couples in Burkina Faso.
2.Glucose-6-phosphate dehydrogenase (G6PD) deficiency is associated with asymptomatic malaria in a rural community in Burkina Faso.
Abdoul Karim OUATTARA ; Cyrille BISSEYE ; Bapio Valery Jean Télesphore Elvira BAZIE ; Birama DIARRA ; Tegwindé Rebeca COMPAORE ; Florencia DJIGMA ; Virginio PIETRA ; Remy MORET ; Jacques SIMPORE
Asian Pacific Journal of Tropical Biomedicine 2014;4(8):655-658
OBJECTIVETo investigate 4 combinations of mutations responsible for glucose-6-phosphate dehydrogenase (G6PD) deficiency in a rural community of Burkina Faso, a malaria endemic country.
METHODSTwo hundred individuals in a rural community were genotyped for the mutations A376G, G202A, A542T, G680T and T968C using TaqMan single nucleotide polymorphism assays and polymerase chain reaction followed by restriction fragment length polymorphism.
RESULTSThe prevalence of the G6PD deficiency was 9.5% in the study population. It was significantly higher in men compared to women (14.3% vs 6.0%, P=0.049). The 202A/376G G6PD A- was the only deficient variant detected. Plasmodium falciparum asymptomatic parasitaemia was significantly higher among the G6PD-non-deficient persons compared to the G6PD-deficient (P<0.001). The asymptomatic parasitaemia was also significantly higher among G6PD non-deficient compared to G6PD-heterozygous females (P<0.001).
CONCLUSIONSThis study showed that the G6PD A- variant associated with protection against asymptomatic malaria in Burkina Faso is probably the most common deficient variant.